Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Default user image.

Åke Lernmark

Principal investigator

Default user image.

The pancreatic β cell recognition of insulin secretagogues : does cyclic AMP mediate the effect of glucose?

Author

  • B. Hellman
  • L. A. Idahl
  • A. Lernmark
  • I. B. Taljedal

Summary, in English

Insulin release and the content of cAMP were studied in microdissected pancreatic islets of non inbred ob/ob (obese) mice. In the absence of 3 isobutyl 1 methylxanthine, a phosphodiesterase inhibitor, 20 mM glucose had no effect on cAMP save a very small initial rise detectable by a freeze stop perifusion technique only. However, combined with this methylxanthine, 20 mM glucose produced significant increases of cAMP both in perifused islets and in islets conventionally incubated in closed vials. Glucose shared this capacity to raise the cAMP level with D glyceraldehyde and 1,3 dihydroxyacetone. Isobutylmethylxanthine (0.05-1.0 mM) or 5 μg/ml of cholera toxin, an activator of adenylate cyclase, also increased the islet cAMP level; the effects of the methylxanthine, whether or not combined with cholera toxin, were potentiated by glucose. Isobutylmethylxanthine (0.05-1.0 mM) or 5 μg/ml of cholera toxin potentiated insulin release in response to 20 mM glucose. However, only 0.5-1.0 mM isobutylmethylxanthine stimulated insulin release in the presence of 3 mM glucose, whereas 0.05-0.1 mM isobutylmethylxanthine or 5 μg/ml of cholera toxin had no effect on secretion at the low glucose concentration. These discrepancies between cAMP promoting and insulin releasing activities suggest that glucose does not initiate insulin release by activating the β cell adenylate cyclase. By being metabolized in the β cells, glucose may both create a release initiating signal not identical with cAMP and enhance cAMP formation, leading to potentiation of the effect of the initiator signal.

Publishing year

1974-01-01

Language

English

Pages

3405-3409

Publication/Series

Proceedings of the National Academy of Sciences of the United States of America

Volume

71

Issue

9

Document type

Journal article

Publisher

National Acad Sciences

Status

Published

ISBN/ISSN/Other

  • ISSN: 0027-8424